CLDN11

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CLDN11

A gene on chromosome 3q26.2-q26.3 that encodes claudin-11, an integral membrane protein of the claudin family, the members of which form a physical barrier that prevents solutes and water from passing freely into the interstitial space between epithelial or endothelial cell sheets, and play critical roles in maintaining cell polarity and signal transduction. Claudin-11 is a major component of CNS myelin and plays a key role in regulating proliferation and migration of oligodendrocytes.
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References in periodicals archive ?
Furthermore, follicle-stimulating hormone (FSH) inhibits the expression of Claudin-11 in vitro [11] and gonadotropin-releasing hormone (GnRH) can regulate the organization of TJ protein in vivo [12].
This study was designed to evaluate the left testis morphology, germ cell apoptosis, sperm count, the expression of Sertoli cell TJ proteins (Occludin, Claudin-11, and ZO1), changes in cytokine (TGF-[beta]3 and TNF-[alpha]) and T levels in the left testicular tissue, and GnRH, FSH, LH, T, INHB, and antisperm antibody (AsAb) serum levels.
Denatured protein (80 [micro]g) was separated by SDS-PAGE gel electrophoresis accompanied with 210 kDa to 10 kDa weight prestained protein ladder and transferred onto polyvinylidene difluoride membrane (PVDF) for immunodetection using primary antibodies against Occludin (1 : 200), Claudin-11 (1:250), ZO-1 (1:100), and [beta]-actin (1:1000).
Figures 4(a) and 4(b) show that experimental varicocele decreased the expression of TJ proteins, Occludin, Claudin-11, and ZO-1, while MOP increased their expression.
MOP could increase the level of Occludin, Claudin-11, and ZO I, decrease the level of AsAb in the serum, and repair the damaged TJ structure and function.
As a result, we believe that TGF-[beta]3 and TNF-[alpha] might be involved in the downregulation of TJ proteins, Occludin, Claudin-11, and ZO-1, and in the damage of the TJ structure that occurred in experimental varicocele.
Background: Claudin-5, claudin-9, and claudin-11 are expressed in endothelial cells to constitute tight junctions, and their deficiency may lead to hyperpermeability, which is the initiating process and pathological basis of cardiovascular disease.
It is extracted, concentrated, and freeze-dried from a group of herbal medicines, such as ginseng, radix paeoniae rubra, borneol, and spiny jujube seed, which contains multiple active components that may be responsible for its antianginal effects.[sup][16],[17],[18] However, the protective mechanism of TXL has not been clarified.[sup][19],[20] Furthermore, we have found that the effect of TXL is on microvascular endothelial cells.[sup][21],[22],[23] Although TXL has been reported to have positive effects on the hypoxia-inhibited claudin-1,[sup][24],[25] whether TXL regulates claudin-5, claudin-9, and claudin-11, which are expressed in the endothelial cells, has not been explored.
To investigate whether TXL modulate claudin-9 and attenuate cell injury in hypoxia, the cells were exposed to hypoxia and treated with TXL and then the messenger RNA (mRNA) expression of claudin-5, claudin-9, and claudin-11 was examined by real-time reverse transcription-polymerase chain reaction (RT-PCR), the claudin-9 protein content was evaluated by western blotting, the claudin-9 distribution was evaluated by immunofluorescence, and cell morphological changes were observed in light microscope.
After the hypoxia-stimulated cells were treated with TXL for 24 h, the mRNA expression of claudin-5, claudin-9, and claudin-11 was measured.
The mRNA expression of claudin-5, claudin-9, and claudin-11 was quantified by real-time RT-PCR.
Vu et al., "OSP/ claudin-11 forms a complex with a novel member of the tetraspanin super family and [beta]1 integrin and regulates proliferation and migration of oligodendrocytes," Journal of Cell Biology, vol.